scholarly journals Kidney-Replenishing Herb Induces SOCS-3 Expression via ERK/MAPK Pathway and Improves Growth of the First-Trimester Human Trophoblast Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-12
Author(s):  
Chang-ying Xing ◽  
De-xiang Zhang ◽  
Sui-qi Gui ◽  
Min-fang Tao
Keyword(s):  
Mapk Pathway ◽  
Recurrent Miscarriage ◽  
First Trimester ◽  
Mek Inhibitor ◽  
Biological Functions ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Mitogen Activated Protein ◽  
Human Trophoblast Cells

Kidney-replenishing herb is a traditional medicine formula in China which has been widely used for clinical treatment of recurrent miscarriage. Our previous study showed that Kidney-replenishing herb could promote proliferation and inhibit apoptosis of the human first-trimester trophoblasts. In the present study, we further explored the potential mechanism and signal pathway of Kidney-replenishing herb on human trophoblast cells. Our research showed that Kidney-replenishing herb stimulated proliferation and reduced apoptosis of human trophoblast cells in vitro, and this appeared to be positive correlation with SOCS-3 transcription, suggesting that Kidney-replenishing herb regulated biological functions of human trophoblast cells by inducing SCOS-3 expression. Furthermore, the Kidney-replenishing herb treatment stimulated the phosphorylation of ERK1/2, and blocking the signaling pathway by mitogen-activated protein MAPK (MEK) inhibitor, U0126, inhibited Kidney-replenishing herb-induced SOCS-3 transcription, depressed proliferation, and promoted apoptosis of human trophoblasts. Kidney-replenishing herbs still induced ERK1/2 phosphorylation after SOCS-3 siRNA silence. Overexpression of SOCS-3 stimulated the proliferation of trophoblast. These findings suggest that SOCS-3 expression is induced by Kidney-replenishing herbs via activation of MAPK pathways, and this may possibly be involved in promoting human trophoblast cells growth which is contributed to embryo development.

Modulation of pp60c-src activity and cellular localization during differentiation of human trophoblast cells in culture

1993 ◽  
Vol 105 (3) ◽  
pp. 629-636 ◽  
Author(s):  
C. Rebut-Bonneton ◽  
S. Boutemy-Roulier ◽  
D. Evain-Brion
Keyword(s):  
Tyrosine Kinase ◽  
Cellular Localization ◽  
Kinase Activity ◽  
Cell Aggregation ◽  
Trophoblast Cells ◽  
Tyrosine Kinase Activity ◽  
Human Trophoblast ◽  
Human Trophoblast Cells ◽  
E Cadherin

The morphological and functional differentiation of human trophoblast cells ends with the formation of terminally differentiated multinucleated syncytial trophoblasts. This in vivo differentiation is mimicked in vitro during the primary culture of extravillous cytotrophoblasts: isolated mononuclear cytotrophoblasts aggregate and fuse to form syncytia. This in vitro differentiation is associated with an increase in epidermal growth factor receptor (EGF-R) expression and a transitory increase in E-cadherin expression during cell aggregation. In the present study, we investigated the expression of pp60c-src during morphological differentiation of trophoblast cells. Cultures were terminated at various time intervals and pp60c-src was analysed by immunocytochemistry using a specific antibody. In addition, pp60c-src was investigated by western blot analysis and its tyrosine kinase activity was measured concomitantly. In mononuclear cytotrophoblasts, pp60c-src was localized at cell-matrix contacts and during the aggregation of cytotrophoblasts, pp60c-src was distributed on the cell surface at points of cell-cell contact being colocalized with EGF-R and E-cadherin. The kinase activity of the pp60c-src protein increased significantly at day 2 when cells were completely aggregated and started to fuse, and remained elevated while cells underwent further differentiation. Inhibition of pp60c-src by herbimycin A at 0.25 to 1 microgram/ml during the first day of culture was associated with a decreased expression of tyrosine kinase activity of EGF-R and an increase in E-cadherin expression. These data suggest that pp60c-src is involved in the modulation of trophoblast cell aggregation and fusion leading to syncytial formation.

Effect of a Soluble Factor Secreted From Cultured Human Trophoblast Cells on In Vitro Lymphocyte Reactions

1987 ◽  
Vol 13 (4) ◽  
pp. 121-124 ◽  
Author(s):  
FUMITAKA SAJI ◽  
MASAYASU KOYAMA ◽  
TAKASHI KAMEDA ◽  
TAKAO NEGORO ◽  
KARO NAKAMURO ◽  
...  
Keyword(s):  
Soluble Factor ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Human Trophoblast Cells

Differentiation of human trophoblast cells in vitro stimulated by extracellular matrix

Placenta ◽  
1993 ◽  
Vol 14 ◽  
pp. 181-200
Author(s):  
Hans-Peter Hohn ◽  
Larry R. Boots ◽  
Hans-Werner Denker ◽  
Magnus Höök
Keyword(s):  
Extracellular Matrix ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Human Trophoblast Cells

Immunoregulatory activity in supernatants from cultures of normal human trophoblast cells of the first trimester

1989 ◽  
Vol 161 (2) ◽  
pp. 446-453 ◽  
Author(s):  
Mrinal K. Sanyal ◽  
Charles J. Brami ◽  
Paul Bischof ◽  
Edwina Simmons ◽  
Eytan R. Barnea ◽  
...  
Keyword(s):  
First Trimester ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Normal Human ◽  
Human Trophoblast Cells

scholarly journals Moderate Hypoxia Down-Regulates Interleukin-6 Secretion and TLR4 Expression in Human Sw.71 Placental Cells

2015 ◽  
Vol 36 (6) ◽  
pp. 2149-2160 ◽  
Author(s):  
Koumei Shirasuna ◽  
Narumi Shimamura ◽  
Kotomi Seno ◽  
Ayaka Ohtsu ◽  
Shogo Shiratsuki ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Ros Production ◽  
Tlr4 Expression ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Moderate Hypoxia ◽  
Hypoxic Conditions ◽  
Markers Of Inflammation ◽  
Human Trophoblast Cells

Background/Aims: The placenta is a vital organ for pregnancy. Many in vitro placental experiments are conducted under 21% O2; however, O2 tension could influence cellular functions, including cytokine secretion. We investigated the effects of oxygen tension between moderate hypoxia (5% O2) and normoxia (21% O2) by testing the hypothesis that moderate hypoxia regulates cellular phenotypes differently from normoxia in human trophoblast cells. Methods and Results: Sw.71 trophoblast cells were incubated under normoxic or moderately hypoxic conditions. Cells were also treated with lipopolysaccharide (LPS) as a Toll-like receptor 4 (TLR4) ligand inducing inflammation. Interleukin-6 (IL-6) as an inflammatory cytokine was determined, and TLR4, hypoxia-induced factor-1α (HIF1α), and reactive oxygen species (ROS) production were detected. Moderate hypoxia increased HIF1α expression and cell proliferation and acted by two different mechanisms to decrease IL-6 secretion compared with normoxia: it limits the TLR4 expression and ROS production. Treatment with cobalt chloride as an HIF1 activator inhibited IL-6 secretion and TLR4 expression; this effect was reversed on treatment with PX-12 as an HIF1 suppressor. Conclusion: IL-6 secretion, TLR4 expression, and ROS production, classical markers of inflammation, are down-regulated by moderate hypoxia, and HIF1α and ROS have a potential to regulate these responses in human trophoblast cells.

scholarly journals MEK-inhibitor-mediated rescue of skeletal myopathy caused by activating Hras mutation in a Costello syndrome mouse model

2021 ◽  
Author(s):  
William E. Tidyman ◽  
Alice F. Goodwin ◽  
Yoshiko Maeda ◽  
Ophir D. Klein ◽  
Katherine A. Rauen
Keyword(s):  
Mouse Model ◽  
Mapk Pathway ◽  
Mek Inhibitor ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Costello Syndrome ◽  
Skeletal Myopathy ◽  
Mitogen Activated Protein

Costello syndrome (CS) is a congenital disorder caused by heterozygous activating germline HRAS mutations in the canonical Ras/mitogen-activated protein kinase (Ras/MAPK) pathway. CS is one of the RASopathies, a large group of syndromes due to mutations within various components of the Ras/MAPK pathway. An important part of the phenotype that greatly impacts quality of life is hypotonia. To gain a better understanding of the mechanisms underlying hypotonia in CS, a mouse model with an activating HrasG12V allele was utilized. We identified a skeletal myopathy that was due in part to an inhibition of embryonic myogenesis and myofiber formation, resulting in a reduction of myofiber size and number that led to reduced muscle mass and strength. In addition to hyperactivation of the Ras/MAPK and PI3K/AKT pathways, there was a significant reduction of p38 signaling, as well as global transcriptional alterations consistent with the myopathic phenotype. Inhibition of Ras/MAPK pathway signaling using a MEK inhibitor rescued the HrasG12V myopathy phenotype both in vitro and in vivo, demonstrating that increased MAPK signaling is the main cause of the muscle phenotype in CS.

In Vitro Restoration of Functional SMN Protein in Human Trophoblast Cells Affected by Spinal Muscular Atrophy by Small Fragment Homologous Replacement

2005 ◽  
Vol 0 (0) ◽  
pp. 050701034702010
Author(s):  
Federica Sangiuolo ◽  
Antonio Filareto ◽  
Paola Spitalieri ◽  
Maria Lucia Scaldaferri ◽  
Ruggiero Mango ◽  
...  
Keyword(s):  
Spinal Muscular Atrophy ◽  
Muscular Atrophy ◽  
Small Fragment ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Smn Protein ◽  
Human Trophoblast Cells
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